Abstract Delayed perforation is a rare but serious complication following endoscopic resection of colonic lesions; however, its pathogenesis remains unclear. We hypothesized that its mechanism mirrors Jackson’s burn model, where a zone of stasis progresses to a zone of coagulation, ultimately leading to perforation. In this study, thermal injury was endoscopically induced in rat colons, and histopathological changes were analyzed at 12-hour intervals. To assess the role of bacterial infection, pseudo-germ-free rats were established by administering a course of antibiotics. The incidence of delayed colonic perforation was compared between the control and pseudo-germ-free rats. Degeneration and thinning of the muscularis propria persisted for 36 hours post-injury, with destruction of this layer observed at 48 hours. Dilated vessels in the mucosa and submucosa peaked at 24 hours, forming a zone of stasis. By 36 hours, mucosal necrosis had intensified, myeloperoxidase-positive cells had increased in the submucosa, and Escherichia coli had translocated into deeper layers, coinciding with expansion of the zone of coagulation. Moreover, pseudo-germ-free rats exhibited significantly fewer perforations. These findings suggest that delayed colonic perforation follows a pathological process similar to thermal burns and that bacterial infection accelerates this progression. Therefore, local infection control may be essential for preventing this serious complication.
Sakae et al. (Sun,) studied this question.